The present invention relates to determinations of relative muscular reflex activity during contractions and lengthenings of the body muscle involved as reflected in corresponding electromyographic signals and, more particularly, to such determinations made when the muscular contractions and extensions are involved with rotations of skeletal joints.
The control of the contracting and lengthening of muscles in the human body has long been known to have both a volitional aspect involving the central portions of the central nervous system and a reflex aspect involving peripheral portions of the central nervous system. In this latter aspect, the stretching of a typical muscle is sensed by a muscle spindle embedded therein and signals indicating such stretching are provided over afferent neurons to the system of spinal neurons. From there, return signals are provided over the alpha motor neurons, or efferent neurons, to the muscle body causing it to contract to counteract the initial stretching. This "local" feedback loop is the basis of reflex actions in the muscle involved.
In the former, or volitional, control aspect, a first mode of control has signals from the central portion of the central nervous system provided along the spinal nerve complex into the peripheral portion of the central nervous system. From there they are transmitted over alpha motor neurons to the muscle body to again cause it to contract.
However, the central portion of the central nervous system is also known to be able to affect or modulate the reflex actions of such a muscle. Thus, the level of signals in the reflex feedback loop described above appear subject to being increased (or decreased) under control of the central portion, i.e. in effect, the "gain" of that control loop can be changed by the central portion. Such a change in this stretch reflex feedback loop gain, i.e. modulation of the stretch reflex, is thought possibly to be due to signals provided from the central portion to the gamma motor neuron which extends to the muscle spindle or to influences exerted by the central portion on loop neurons (or interneurons) in the spinal nerve complex. Whatever the means, there is substantial evidence that movement of the muscle under volitional control is given effect not only through direct signals transmitted from the central portion of the central nervous system through the spinal nerves and over the alpha motoneuron to the muscle, but also through the central portion transmitting signals having the effect of modulating the stretch reflex.
As is well known, muscles in moving structural portions of which they are comprised, and other bodily structures to which such muscles are connected, are capable of being forced to contract in length but, in the other direction, are merely permitted to lengthen under some externally applied tensile force. That is, lengthening of a muscle cannot be forced solely by signals transmitted over motor neurons to that muscle. Thus, skeletal joints in the human body are operated by pairings of muscles to permit them to be rotated in opposite directions.
A member of such a muscle pair for such a skeletal joint is provided more or less on opposite sides of that joint and each is capable of rotating the actuator portion of that joint, with respect to the base portion of that joint, under a forced contraction thereof toward itself. Hence, each member of that muscle pair can cause a rotation of the actuator portion of that joint in a direction opposite to that which the other member can cause a rotation to occur under a forced contraction of that member. Thus, normal control of the rotation of an actuator portion of a skeletal joint with respect to its base portion requires that the contracting muscle on the side of the joint toward which the actuator portion is drawn during its contraction, or the agonist muscle, be accompanied by the absence of any significant contracting activity in the muscle on the opposite side of the joint, or the antagonist muscle.
Thus, a volitional movement of the agonist muscle to rotate the actuator portion of the skeletal joint toward it requires signals from the central portion of the central nervous system to be directly sent to the agonist muscle without a similar direct signal sent to the antagonist muscle. In addition, the stretch reflex modulation directed by the central portion is to be concomitantly increased in the agonist muscle but should not be increased in the antagonist muscle, or should be inhibited in this antagonist muscle. That is, co-contraction of the agonist and antagonist muscles should be avoided for proper rotation in most circumstances of the actuator portion of the joint. To this end, there is evidence of reciprocal inhibition being associated with the stretch reflex in the human body so that stretch reflex modulation associated with the agonist muscle is accompanied by an inhibition of that reflex in the antagonist muscle.
There are, unfortunately, many situations in which proper control of rotations of a skeletal joint in the human body is lacking or degraded. Among the movement disorders associated with the skeletal joints are spasticity, dystonia, cerebellar hypotonia, and bradykinesia, with this latter term referring to the abnormalities of volitional movement evident in some sufferers of Parkinson's disease. Bradykinesia refers to a variety of volitional movement difficulties including slow onset of movement with respect to a given stimulus, reduced amplitude of movement in reaching a goal position after a stimulus, reduced peak velocity of such movements, and rapid fatigue occurring with repetitive movements. Bradykinesia is considered to be independent of the other major groupings of symptoms associated with Parkinson's disease, muscular rigidity and resting tremors. Concerning these symptom types, bradykinesia is a major factor responsible for the disability experienced by those suffering from Parkinson's disease.
Just what defects in the central nervous system that are caused by Parkinson's disease also lead to bradykinesia has not been well understood. Studies of rapid joint movements, or ballistic movements, have demonstrated that abnormalities occur both in associated electromyographic signals and in the movements themselves in those suffering from Parkinson's disease. Studies based on having sufferers of this disease operating one of their skeletal joints to track a target based on visual guidance have also demonstrated defects in such sufferers' performance at those kinds of tasks. Much of the evidence uncovered in such studies have been used to implicate defects in the central portion of the central nervous system as the cause of bradykinesia.
However, studies of sufferers of Parkinsonism, based on supplying a stimulus to initiate volitional movement, have shown that changes with respect to those not so suffering in reaction time to that stimulus, or the time duration to first movement thereafter, are independent of the increases in total movement time following such a stimulus for the actuator portion of the joint to reach a position goal. This suggests that even though the volitional signals have been clearly provided from the central portion of the central nervous system to the muscles controlling the joint, there are also difficulties in the peripheral portion of the central system retarding the carrying out of the desired motion by sufferers of Parkinson's disease.
There has recently been found evidence indicating that a defect or defects in the stretch reflex during the execution of a skeletal joint movement may be responsible for at least some aspects of bradykinesia. There is evidence suggesting that such a volitional movement, which should be based on coordinated direct signals from the central portion of the central nervous system to the agonist muscle involved and indirect signals from that central portion to modulate its stretch reflex, are not properly coordinated in achieving a desired motion. Such a lack of coordination provides the possibility of the agonist and antagonist muscles associated with the skeletal joint having overlapping contracting activity so that one is braking the activity of the other to an extent. A determination of the extent of such braking, for purposes of determining the extent of bradykinesia in Parkinson's disease in the sufferer, would be desirable. In addition, such a determination could be used to evaluate therapeutic strategies and to set levels of pharmacologic therapy.